July 2007 - Posts
I've been exploring these kinds of services lately. Anything that further simplifies personal publishing, I'm interested. I've set up a quick mirror of processofchange.com: http://bobreb.wetpaint.com/.
I managed to pull a nice size rainbow out of this section (my secret) of the Skykomish river north of Monroe:
I promised myself last year I do more exploring out Washington's route 2. Lake Serene was my first stop. Here's the topo:
Some facts:
7.2 miles round trip; 2200 ft elevation gain; just past mile marker 35 on US 2.
On the way up we got a glimpse of Bridal Veil falls:
It would be worth a trip back to get up underneath the falls.
The lake was nice:
I jumped and (obviously) did not suffer cardiac arrest -- though it was about as cold as expected. The black flies were out, so the cold water was nice.
The cliffs in the surrounding cirque (I assume this is an actual cirque -- sure looked like one) were impressive. Looked climbable:
Another of the lake, just for fun:
I love the personal publishing revolution. I really do. I was just surfing around the links off my main social network feeds, and I found this interesting perspective.
This is the marketplace of ideas in action.
Among other things (I think I might have an attention problem) I'm reading this:
I'm forcing myself,even though my initial scan didn't suggest it had much to offer, to read this book cover to cover. You see Mr. Keen believes the personal publishing revolution is a disaster. If I don't read his work, if I don't give equal time to competing ideas, then I can't claim I'm benefiting from a marketplace. Rather, I'd be wallowing in an (and soon to be proverbial) echo chamber hearing only my own words.
It was a good morning. I started the day at Calligan Lake. That would be on Hancock private land ($$$ permit required). Here's the topo:
I managed to get on the water by 6:30 AM -- still too late I think. Not much luck -- couple of 6-inchers and one 10 inch trout in the few hours I was kicking around the lake. That's just fine, as it turns out. The lake was beautiful.
It was great to be out on the water, and kicking the boat around is good exercise. I got done early enough that I stopped a favorite spot on the North Fork of the Snoqualmie. I caught lots of little trout.
Both of these spots are on Hancock land. The permit is expensive, but it's worth it. Despite the fact that most of the place looks more like this:
They do a bit of tree cutting...
Recent media hype has it that vitamin E isn't useful. This is based on studies that gave vitamin E to people already old and all messed up with heart failure. No kidding. Try putting oil in your engine after it has burned up for lack thereof. -- BL
Department of Biochemistry and Molecular Biology, School of Medicine, University of Cádiz, Spain. ana.navarro@uca.es
Male mice receiving vitamin E (5.0 g alpha-tocopherol acetate/kg of food) from 28 wk of age showed a 40% increased median life span, from 61 +/- 4 wk to 85 +/- 4 wk, and 17% increased maximal life span, whereas female mice equally supplemented exhibited only 14% increased median life span. The alpha-tocopherol content of brain and liver was 2.5-times and 7-times increased in male mice, respectively. Vitamin E-supplemented male mice showed a better performance in the tight-rope (neuromuscular function) and the T-maze (exploratory activity) tests with improvements of 9-24% at 52 wk and of 28-45% at 78 wk. The rates of electron transfer in brain mitochondria, determined as state 3 oxygen uptake and as NADH-cytochrome c reductase and cytochrome oxidase activities, were 16-25% and 35-38% diminished at 52-78 wk. These losses of mitochondrial function were ameliorated by vitamin E supplementation by 37-56% and by 60-66% at the two time points considered. The activities of mitochondrial nitric oxide synthase and Mn-SOD decreased 28-67% upon aging and these effects were partially (41-68%) prevented by vitamin E treatment. Liver mitochondrial activities showed similar effects of aging and of vitamin E supplementation, although less marked. Brain mitochondrial enzymatic activities correlated negatively with the mitochondrial content of protein and lipid oxidation products (r2 = 0.58-0.99, P < 0.01), and the rates of respiration and of complex I and IV activities correlated positively (r2 = 0.74-0.80, P < 0.01) with success in the behavioral tests and with maximal life span.
Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Plaza Fragela 9, 11003 Cádiz, Spain. ana.navarro@uca.es
Aged mammalian tissues show a decreased capacity to produce ATP by oxidative phosphorylation due to dysfunctional mitochondria. The mitochondrial content of rat brain and liver is not reduced in aging and the impairment of mitochondrial function is due to decreased rates of electron transfer by the selectively diminished activities of complexes I and IV. Inner membrane H(+) impermeability and F(1)-ATP synthase activity are only slightly affected by aging. Dysfunctional mitochondria in aged rodents are characterized, besides decreased electron transfer and O(2) uptake, by an increased content of oxidation products of phospholipids, proteins and DNA, a decreased membrane potential, and increased size and fragility. Free radical-mediated oxidations are determining factors of mitochondrial dysfunction and turnover, cell apoptosis, tissue function, and lifespan. Inner membrane enzyme activities, such as those of complexes I and IV and mitochondrial nitric oxide synthase, decrease upon aging and afford aging markers. The activities of these three enzymes in mice brain are linearly correlated with neurological performance, as determined by the tightrope and the T-maze tests. The same enzymatic activities correlated positively with mice survival and negatively with the mitochondrial content of lipid and protein oxidation products. Conditions that increase survival, as vitamin E dietary supplementation, caloric restriction, high spontaneous neurological activity, and moderate physical exercise, ameliorate mitochondrial dysfunction in aged brain and liver. The pleiotropic signaling of mitochondrial H(2)O(2) and nitric oxide diffusion to the cytosol seems modified in aged animals and to contribute to the decreased mitochondrial biogenesis in old animals.
Creatine, long used by weight lifters to improve workouts, extended the
life span of mice by 9% and reduced age-related brain deterioration.
Creatine monophosphate donates a phosphorus atom to adenosine
diphosphate, which becomes adenosine triphosphate (ATP) the primary
energy carrier in cells. Life is all about energy. Your liver produces
a certain amount of creatine each day. At least in mice, more seems to
be better.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&list_uids=17416441&c
md=Retrieve&indexed=google
The supplementation of creatine (Cr) has a marked neuroprotective
effect in mouse models of neurodegenerative diseases. This has been
assigned to the known bioenergetic, anti-apoptotic, anti-excitotoxic,
and anti-oxidant properties of Cr. As aging and neurodegeneration share
pathophysiological pathways, we investigated the effect of oral Cr
supplementation on aging in 162 aged C57Bl/6J mice. Outcome variables
included "healthy" life span, neurobehavioral phenotyping, as well as
morphology, biochemistry, and expression profiling from brain. The
median healthy life span of Cr-fed mice was 9% higher than in control
mice, and they performed significantly better in neurobehavioral tests.
In brains of Cr-treated mice, there was a trend towards a reduction of
reactive oxygen species and significantly lower accumulation of the
"aging pigment" lipofuscin. Expression profiling showed an upregulation
of genes implicated in neuronal growth, neuroprotection, and learning.
These data show that Cr improves health and longevity in mice. Cr may
be a promising food supplement to promote healthy human aging.
Thought provoking, although perhaps not completely accurate:
http://www.glumbert.com/media/shift